Bone disorders or conditions, such as synostotic conditions or ectopic mineralization most often require highly invasive treatment methodologies.
Cranial suture is soft tissue interface between calvarial bones, and has two primary functions: enabling the longitudinal growth of calvarial bones and serving as relatively immobile articulations. Functionally, cranial sutures are analogous to appendicular growth plate, both of which enable longitudinal bone growth.
Craniosynostosis refers to premature ossification of cranial sutures, and occurs in approximately one of every 2,000 live human births. Children with craniosynostosis may suffer from craniofacial deformities, seizure and mental retardation. The primary treatment for craniosynostosis is surgical craniotomy, with a major goal to relieve abnormally high intracranial pressure. Craniotomy is a traumatic surgery, involving the reshaping of skull bones and removal of synostosed bone of empirical size (Mooney et al. (2004) Expert Opin Biol Ther 4, 279-299). Surgically corrected craniosynostosis may re-fuse, necessitating secondary surgeries.
Recent reports disclose a tissue-engineered cranial suture-like structure and the use of TGFβ3 to modulate synostosed cranial sutures (Hong and Mao (2004) J Dental Res 83, 751-756; Moioli et al. (2006) Tissue Eng 12, 537-546), consistent with the observation that TGFβ3 modulates the fate of both natural and synostosed cranial sutures (Opperman et al. (2002) Orthod Craniofacial Res 5, 5-16). TGFβ3 attenuates not only the osteogenic differentiation of bone marrow derived osteoblasts, but also osteoblastic matrix synthesis (Moioli et al., 2006). However, little is known whether other cytokines also regulate sutural morphogenesis.
Thus, there exists the need for a minimally invasive approach for treatment of bone disorders or conditions.